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Spinal cord injury (SCI) initiates a robust innate immune response at the lesion site which fosters neuroinflammation. Pattern recognition receptors (PRRs) are the principal mediators of neuroinflammation. Toll-like receptors (TLRs) are the best-characterized family of PRRs and they are activated in response to endogenous ligands released by damaged cells following injury. Activation of TLR2 and TLR4 promotes the protection, repair, and functional recovery following SCI. In contrast, antagonism of TLR9 protects injured axons, modulates astrocyte function at the glial scar, polarizes macrophages into a beneficial phenotype, and improves the functional outcomes of SCI. The role of other TLRs in SCI remains elusive and warrants further investigation. Elucidating the cellular and molecular mechanisms underlying TLR signaling in SCI could provide insights into their mode of action in multiple CNS pathologies.